DermatologyTier 1Disease (DEADMAN)

Vitiligo

Description

Acquired, autoimmune destruction of epidermal melanocytes -> well-demarcated depigmented (chalk-white) macules/patches
Non-segmental (generalised) - ~90% - bilateral, symmetric, progressive, associated with other autoimmunity
Segmental - unilateral, dermatomal/blaschkoid distribution, earlier onset, more stable course, less autoimmune association - a mechanistically distinct entity

~0.5-1% of the population, any age but often onset before age 30
No sex predilection; more visually apparent (and stigmatising) in darker skin types

Autoimmune melanocyte destruction - CD8+ cytotoxic T cells target melanocytes, IFN-gamma -> CXCL9/CXCL10 chemokine signalling recruits and amplifies the autoimmune attack (the basis for JAK inhibitor efficacy)
Genetic susceptibility - polygenic, overlaps with other autoimmune disease loci
Koebner phenomenon - new lesions at sites of skin trauma/friction
Segmental subtype - thought to involve a somatic mosaicism/localised mechanism rather than systemic autoimmunity, explaining its more stable, non-progressive course

Clinical

Well-demarcated, depigmented (not hypopigmented) macules - Wood's lamp examination enhances contrast, useful in fair skin/early lesions
Symmetric distribution favouring periorificial (eyes, mouth), acral (hands/feet), and flexural sites (non-segmental); dermatomal for segmental
Diagnosis usually clinical; biopsy rarely needed (absent melanocytes on histology if done)

Screen for associated autoimmunity (non-segmental)

Thyroid disease (autoimmune thyroiditis) - commonest association, check TFTs/thyroid antibodies
Consider screening for other autoimmune disease if symptomatic (T1DM, pernicious anaemia, Addison's disease, alopecia areata)

A. First-line topical (limited disease)

Potent topical corticosteroid or topical calcineurin inhibitor (tacrolimus) - face/flexures particularly responsive; calcineurin inhibitors preferred for facial disease to avoid steroid atrophy
Topical ruxolitinib (JAK inhibitor) cream - now an approved first-line option, particularly for facial vitiligo, superior repigmentation response vs vehicle in trials

B. More extensive/refractory disease

Phototherapy - narrowband UVB - first-line for widespread disease, often combined with topical agents (combination more effective than either alone)
Systemic/oral JAK inhibitors - emerging option for extensive refractory disease, evidence evolving

C. Stable, long-standing depigmentation

Surgical techniques (melanocyte-keratinocyte transplantation, mini-punch grafting) for stable segmental or localised non-segmental disease not responding to medical therapy
Depigmentation therapy (e.g. monobenzone) - considered for extensive (>50%) disease where achieving uniform skin tone is preferred over further repigmentation attempts

D. Supportive

Camouflage cosmetics, sunscreen (depigmented skin burns easily and lacks the visual cue of tanning)
Psychological support - significant quality-of-life and stigma burden, particularly in darker skin types

Autoimmune thyroid disease - commonest association
Alopecia areata, T1DM, pernicious anaemia, Addison's disease - other autoimmune associations (non-segmental)
Halo naevi - can coexist, marker of active melanocyte autoimmunity
Family history of vitiligo or other autoimmune disease

Non-segmental - typically chronic and progressive, waxing/waning, unpredictable extent; spontaneous repigmentation uncommon and usually partial
Segmental - stabilises early (often within 1-2 years), then remains largely static
Repigmentation with treatment is often partial and slower on acral sites (hands/feet) than face/trunk
Major psychosocial impact independent of physical severity - counselling and support should be integrated early, not offered only after treatment failure

6 more sections, plus exam facts

Premium unlocks every note across every specialty, and the full exam fact library behind it.